Spontaneous skin ulceration and defective T cell function in CD18 null mice.
Spontaneous skin ulceration and defective T cell function in CD18 null mice.
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CD18无效小鼠的自发皮肤溃疡和T细胞功能缺陷。
DOI:
10.1084/jem.188.1.119
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发表时间:
1998-07-06
期刊:
影响因子:
--
通讯作者:
Beaudet AL
中科院分区:
文献类型:
--
作者:
Scharffetter-Kochanek K;Lu H;Norman K;van Nood N;Munoz F;Grabbe S;McArthur M;Lorenzo I;Kaplan S;Ley K;Smith CW;Montgomery CA;Rich S;Beaudet AL
A null mutation was prepared in the mouse for CD18, the β2 subunit of leukocyte integrins. Homozygous CD18 null mice develop chronic dermatitis with extensive facial and submandibular erosions. The phenotype includes elevated neutrophil counts, increased immunoglobulin levels, lymphadenopathy, splenomegaly, and abundant plasma cells in skin, lymph nodes, gut, and kidney. Very few neutrophils were found in spontaneously occurring skin lesions or with an induced toxic dermatitis. Intravital microscopy in CD18 null mice revealed a lack of firm neutrophil attachment to venules in the cremaster muscle in response to N-formyl- methionyl-leucyl-phenylalanine. A severe defect in T cell proliferation was found in the CD18 null mice when T cell receptors were stimulated either by staphylococcal enterotoxin A or by major histocompatibility complex alloantigens demonstrating a greater role of CD11/CD18 integrins in T cell responses than previously documented. The null mice are useful for delineating the functions of CD18 in vivo.